scholarly journals Tumour necrosis factor induces phosphorylation primarily of the nitric-oxide-responsive form of glyoxalase I

2007 ◽  
Vol 407 (1) ◽  
pp. 121-128 ◽  
Author(s):  
Virginie de Hemptinne ◽  
Dieter Rondas ◽  
Joël Vandekerckhove ◽  
Katia Vancompernolle
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
No Synthase ◽  
Dominant Factor ◽  
Glyoxalase I ◽  
No Donor ◽  
Necrosis Factor ◽  
Tnf Tumour Necrosis Factor

We have previously shown that TNF (tumour necrosis factor) induces phosphorylation of GLO1 (glyoxalase I), which is required for cell death in L929 cells. In the present paper, we show that the TNF-induced phosphorylation of GLO1 occurs primarily on the NO (nitric oxide)-responsive form of GLO1. In addition, analysis of several cysteine mutants of GLO1 indicated that Cys-138, in combination with either Cys-18 or Cys-19, is a crucial target residue for the NO-mediated modification of GLO1. Furthermore, the NO-donor GSNO (S-nitrosogluthathione) induces NO-mediated modification of GLO1 and enhances the TNF-induced phosphorylation of this NO-responsive form. GSNO also strongly promotes TNF-induced cell death. By the use of pharmacological inhibition of iNOS (inducible NO synthase) and overexpression of mutants of GLO1 that are deficient for the NO-mediated modification, we have shown that the NO-mediated modification of GLO1 is not a requirement for TNF-induced phosphorylation or TNF-induced cell death respectively. In summary, these data suggest that the TNF-induced phosphorylation of GLO1 is the dominant factor for cell death.

PS-145-Albumin protects the liver from tumour necrosis factor alpha-induced cell death

2019 ◽  
Vol 70 (1) ◽  
pp. e92
Author(s):  
Marta Duran-Güell ◽  
Mireia Casulleras ◽  
Roger Flores-Costa ◽  
Cristina López-Vicario ◽  
Esther Titos ◽  
...  
Keyword(s):  
Cell Death ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Tumour Necrosis Factor Alpha ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

scholarly journals CD40 and tumour necrosis factor‐α co‐operate to up‐regulate inducuble nitric oxide synthase expression in macrophages

Immunology ◽  
2012 ◽  
Vol 135 (2) ◽  
pp. 140-150 ◽  
Author(s):  
Jose‐Andres C. Portillo ◽  
Luis Muniz Feliciano ◽  
Genevieve Okenka ◽  
Frederick Heinzel ◽  
M. Cecilia Subauste ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Tumour Necrosis Factor Α ◽  
Factor Α ◽  
Oxide Synthase ◽  
Necrosis Factor

Hyperdynamic Circulation of Cirrhotic Rats with Ascites: Role of Endotoxin, Tumour Necrosis Factor-α and Nitric Oxide

1997 ◽  
Vol 93 (3) ◽  
pp. 219-225 ◽  
Author(s):  
Chi-Jen Chu ◽  
Fa-Yauh Lee ◽  
Sun-Sang Wang ◽  
LU Rei-Hwa ◽  
Yang-Te Tsai ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Tumour Necrosis Factor ◽  
Plasma Levels ◽  
Tumour Necrosis ◽  
Colorimetric Assay ◽  
Plasma Concentrations ◽  
No Production ◽  
Hyperdynamic Circulation ◽  
Tnf Α ◽  
Necrosis Factor

1. Hyperdynamic circulation observed in portal hypertensive states is characterized by generalized vasodilatation, increased cardiac index and increased systemic and regional blood flows. Endotoxin, tumour necrosis factor-alpha (TNF-α) and nitric oxide (NO) have been reported to be involved in the pathogenesis of hyperdynamic circulation, but the interactions between endotoxin, TNF-α and NO in cirrhotic rats with ascites have never been specifically addressed. 2. This study was designed to determine systemic and portal haemodynamics and plasma levels of endotoxin, TNF-α and nitrate/nitrite in cirrhotic rats with ascites and investigate the relationships between these substances. 3. Plasma concentrations of endotoxin, TNF-α and nitrate/nitrite (an index of NO production) were determined in 25 cirrhotic rats with ascites and 17 control rats using the Limulus assay, ELISA and a colorimetric assay respectively. In addition, haemodynamic studies were performed in another ten cirrhotic rats with ascites and ten control rats. 4. Cirrhotic rats with ascites had hyperdynamic circulation accompanied by increased plasma levels of endotoxin, TNF-α and nitrate/nitrite, as compared with control rats. Significant correlation existed between plasma levels of endotoxin and nitrate/nitrite (r = 0.59, P < 0.0001) and between plasma levels of endotoxin and TNF-α (r = 0.63, P < 0.0001). No correlation was detected between plasma levels of TNF-α and nitrate/nitrite (r = 0.24, P > 0.05). 5. This study suggests that endotoxaemia developed in cirrhotic rats with ascites may stimulate NO formation directly or indirectly via cytokine cascade, and consequently participate in the development and/or maintenance of hyperdynamic circulation.

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